Abstract: Case Reports |


Nauman A. Chaudary, MBBS*; Melanie Fisher, MD; Luis Teba, MD
Author and Funding Information

West Virginia University School of Medicine, Morgantown, WV


Chest. 2005;128(4_MeetingAbstracts):476S-a-477S. doi:10.1378/chest.128.4_MeetingAbstracts.476S-a
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INTRODUCTION:  Hantavirus Pulmonary Syndrome (HPS) may lead to respiratory distress, hemodynamic compromise, and noncardiogenic pulmonary edema. High-Frequency Oscillatory Ventilation (HFOV) is an alternative mode of ventilatory support for patients with severe adult respiratory distress syndrome (ARDS). We present a severe case of HPS who did not respond to conventional ventilation. He was treated with HFOV, and recovered.

CASE PRESENTATION:  A 41 year old man, presented with fever, headache, myalgias, dyspnea, and hematuria. He removed rodent droppings at a cabin in rural West Virginia two weeks earlier. He developed respiratory distress, and was intubated. Chest radiographs showed bilateral infiltrates (Figure 1). All cultures including bronchoalveolar lavage fluid were negative. Hantavirus-specific IgM and IgG antibodies were positive, and confirmed by the CDC. One day after intubation, PaO2 was 62 mmHg on pressure control ventilation (PCV), FIO2 1, and PEEP 14 cmH2O. Then, the ventilator was changed to HFOV, and oxygenation improved, but his blood pressure decreased, and he required fluids boluses, vasopressors, and a pulmonary artery catheter. The initial HFOV settings were mean airway pressure of 35 cmH2O, frequency 5 Hz, and amplitude 100 cmH2O. On subsequent days, he remained hypotensive and with low cardiac output. Pulmonary overdistension was suspected. HFOV was held for a few seconds, and a sudden improvement in hemodynamics was observed (table 1). Afterward, HFOV settings were adjusted. He developed multiple organ failure. CVVHD and anticoagulation were started. During the 2nd week in ICU, his PaCO2 level continued to rise (pH 7.13, and PaCO2 71 mmHg), and oxygen saturation dropped to 88% on FIO2 1. Pneumothorax was ruled out, and an emergent bronchoscopy was performed. A large amount of thick mucus obstructing lobar and segmental divisions in both lungs was observed and removed. This resulted in a sudden increase in oxygen saturation to 98%. At the end of the procedure pH was 7.21, PaCO2 51 mmHg, and PaO2 87 mmHg. After 10 days of HFOV, his clinical course improved slowly, and he was eventually discharged.

DISCUSSIONS:  HPS carries a high mortality rate. In the USA, it is usually caused by the Sin Nombre virus. It was initially reported in the SW, but sporadic cases have also been observed in other states. It is transmitted by inhalation of contaminated aerosol from excreta of infected rodents. Our patient apparently acquired it while cleaning the cabin. After a three-week incubation period, patients usually present with fever, malaise, and myalgias. As in our patient, these symptoms may be followed by the common clinical characteristics of HPS: fever, thrombocytopenia, hemoconcentration, respiratory compromise, and ARDS. Positive Hantavirus-specific IgM or IgG antibodies confirm the diagnosis. Treatment of HPS includes intensive care support, and initiation of mechanical ventilation if needed. In ARDS, HFOV has been been shown to be safe and effective in improving oxygenation. To our knowledge, the use of HFOV in patients with HPS has not been reported. Barotrauma and hemodynamic compromise are complications of HFOV. The hemodynamic changes result from HFOV induced increase in intrathoracic pressure. In our case, holding of HFOV for a few seconds resulted in a sudden increase in blood pressure and cardiac output. In addition, mucus inspissation is another potential problem with HFOV. The presence of unexplained refractory hypercapnea, as occurred in our patient, should alert the physician for possible endotracheal tube or diffuse airway obstruction, and the need for bronchoscopy.

CONCLUSION:  Intensive critical care support in patients with HPS may lead to a complete recovery. HFOV appeared to be effective in our patient. However, clinicians using this ventilator mode should be aware of the potential deterioration in hemodynamics, and possible diffuse intrapulmonary mucus plugging that HFOV can induce.TABLE 1

Hemodynamic Profile During Conventional Ventilation, High Frequency Oscillatory Ventilation (HFOV) With Mean Airway Pressure (MAP) of 35 cmH2O, and HFOV With MAP 25 cmH2O

CVP(mmHg)PCWP(mmHg)CO(L/min)CI(L/min/m2)BP(mmHg)Conventional Ventilation15146.33.3110/70HFOV (MAP 35 cmH2O )23203.71.985/55HFOV (MAP 25 cmH2O)23245.22.7150/80

CVP = Central Venous Pulse

DISCLOSURE:  Nauman Chaudary, None.

Wednesday, November 2, 2005

2:00 PM- 3:30 PM




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